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Immunology Flashcards

1
Q

Graves disease:

a) What type of autoantibody is produced? (class of Ig)
b) What is the target?
c) What type of hypersensitivity is it?

A

a) IgG
b) TSH receptor
c) II

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2
Q

What antibodies are found in Hashimoto’s thyroiditis, and what class of hypersensitivity is it?

A

Anti-TPO and anti-thyroglobulin

Type II and IV

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3
Q

Which auto antigens are present in T1DM and what type of hypersensitivity is it?

A

Glutamid acid dehydrogenase (GAD), islet antigen 2

Type IV hypersensitivity

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4
Q

What is the consequence of vitamin B12 deficiency?

A

Subacute degeneration of the spinal cord (lateral and dorsal columns), peripheral neuropathy, optic neuropathy.

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5
Q

What are the antibodies found in pernicious anaemia, and what type of hypersensitivity reaction is it?

A

Anti-IF, anti-gastric parietal cell

Type II

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6
Q

What are the antibodies found in myasthenia gravis, and what type of hypersensitivity reaction is it?

A

Anti-acetylcholine receptor

Type II

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7
Q

What unique test is used to confirm myasthenia gravis?

A

tensilon test - inject edrophonium (anticholinesterase) to prolong Ach life to act on residual receptors

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8
Q

What is the antibody seen in goodpasture disease and what is its pattern of deposition?

A

Anti-GBM

Smooth linear deposition

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9
Q

What type of nephritis is seen in good pastures, and what type of hypersensitivity reaction is it?

A

Crescentic nephritis

Type II

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10
Q

Is ANCA positive or negative in Goodpastures disease?

A

Negative

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11
Q

Which HLA type is associated with rheumatoid arthritis?

A

HLA DR4 and DR1

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12
Q

What is the pathophysiology of RA?

A
  • peptidylarginine deiminases (PAD) type 2 and 4 convert arginine to citrulline
  • polymorphisms associated with increased citrullination
  • HLA DR4/DR1 present citrullinated peptides
  • Antibodies against citrullinated proteins (loss of tolerance)
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13
Q

Which antibodies are found in RA, and what type of hypersensitivity reaction does it involve?

A

Anti-CCP (cyclic citrullinated peptide)
Anti-RF
Type II, III and IV

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14
Q

What is Anti-RF?

A

IgM against IgG (RF)

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15
Q

Which conditions are associated with anti nuclear antibodies?

A

SLE, sjogren’s syndrome, systemic sclerosis, dermato/polymyositis

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16
Q

Which antibodies are found in SLE, and what type of hypersensitivity reaction does it involve?

A

Anti-dsDNA

Type III hypersensitivity

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17
Q

What are anti-ENA antibodies and give some examples

A

Anti-extractable nuclear antigens:

  • Ribonucleoproteins (Ro, La, Sm, RNP)
  • Enzymes (RNA polymerase, topoisomerase)
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18
Q

Which complement components are affected during active and severe SLE?

A

Active: reduced C4

Severe active: reduced C4 and C3

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19
Q

Which antibodies are present in sjogren’s syndrome?

A

Anti-Ro, anti-La

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20
Q

Which antibodies to test for in antiphopholipid syndrome?

A

Anticardiolipid

Lupus anticoagulant

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21
Q

What is the difference between limited cutaneous systemic sclerosis and diffuse?

A

Limited: anticentromere antibodies, skin involvement not past forearms (but can involve personal)
Diffuse: antitopoisomerase (Scl70) antibodies, more extensive GI disease, interstitial pulmonary disease, scleroderma kidney

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22
Q

What type of hypersensitivity reactions are dermatomyositis and polymyositis?

A

Dermato: III
Poly: IV

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23
Q

Which antibody is associated with idiopathic inflammatory myopathy?

A

Anti-Jo1

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24
Q

What size vessels are affected in ANCA-associated vasculitis?

A

Small vessels

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25
Q

Name the 3 ANCA-associated vasculitides

A

Microscopic polyangiitis
Granulomatosis with polyangiitis (Wegener’s)
Eosinophilic granulomatosis with polyangiitis (Churg strauss)

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26
Q

Name 2 large-vessel systemic vasculitides.

A

Takayasu’s arteritis

Giant cell arteritis/polymalgia rheumatica

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27
Q

Name 2 medium vessel systemic vasculitides

A

Polyarteritis nodosa

Kawasaki disease

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28
Q

Name 3 immune-complex associated small vessel systemic vasculitides

A

Anti-GBM disease (Goodpasture’s)
IgA disease
Cryoglobulinaemia

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29
Q

What is the target of c-ANCA?

A

Proteinase 3

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30
Q

What is the target of p-ANCA?

A

Myeloperoxidase

31
Q

Which of the 3 small-vessel ANCA is associated vasculitis is associated with c-ANCA (as opposed to p-ANCA)?

A

Granulomatosis with polyangiitis

32
Q

Which antibody and other condition is associated with UC?

A

p-ANCA

PSC

33
Q

Which HLA allele is most closely associated to coeliac disease?

A

HLA DQ2/8

34
Q

Which is the 1 first-line immunological test for coeliac disease?

A

Anti-TTG

35
Q

What type of antibodies are anti-TTG and anti-endomysial?

A

IgA

36
Q

What are the histopathological features of coeliac disease?

A

Reduced/reversed villous:crypt ratio
Villous atrophy
Crypt hyperplasia
>20 intraepithelial lymphocytes per 100 epithelial cells

37
Q

What malignancy is coeliac associated with?

A

T cell lymphoma

38
Q

Describe the pathway by which gluten causes epithelial damage.

A
  • Gliadin deaminated by TTG and presented to APCs
  • CD4 T cells activated and produce IFNy
  • Leads to IL15 production
  • Activates intraepithelial lymphocytes which kill epithelial cells
39
Q

What are the immune modulatory effects of corticosteroids?

A
  • Inhibit phospholipase A2 (thus prostaglandin formation)
  • Reduce macrophage function
  • Reduce lymphocyte function and promote their apoptosis
40
Q

Why do corticosteroids cause a transient increase in neutrophil counts?

A
  • Decrease expression of adhesion molecules on endothelium

* Block signals involved in moving immune cells from blood to tissue

41
Q

What is the relative proportions of white cells seen in someone soon after taking corticosteroids?

A

High neutrophils, low lymphocytes

42
Q

What are some side effects of cyclophosphamide?

A

o Toxic to proliferating cells – BM depression, hair loss, sterility (M>F)
o Haemorrhagic cystitis – toxic metabolic acrolein excreted via urine
o Malignancy – bladder cancer, haematological malignancies, non-melanoma skin cancer
o Infection – pneumocystis jiroveci

43
Q

What to check before starting someone on azathioprine?

A

TPMT polymorphism

44
Q

Which immunosuppressant is commonly used for systemic autoimmune conditions and vasculitis?

A

Cyclophosphamide

45
Q

Which immunosuppressant increases the risk of infection with JC virus (multifocal leukoencephalopathy) and herpes virus reactivation?

A

Mycophenolate mofetil

46
Q

What is the main limitation of plasmapheresis and how can this be overcome?

A

• Rebound antibody production

Give an anti proliferative agent.

47
Q

Give examples of calcineurin inhibitors, their mechanism of action, and indications of use.

A

Ciclosporin, tacrolimus
Block calcineurin, so less expression of IL2 in T cells, thus less T cell activation/differentiation
Immunosuppresion

48
Q

What are some cell signalling targets of immunosuppressants?

A

Calcineurin
JAK
PDE4

49
Q 
What are the cell surface targets of these immunosuppressants, and the resultant consequence/effect?
•	Basiliximab
•	Abatacept
•	Rituximab 
•	Natalizumab 
•	Tocilizumab
A
  • Basiliximab – anti-CD25 (IL-2 receptor alpha chain). Prevent T cell activation.
  • Abatacept – CTLA4-Ig (binds to CD80 and 86 on APCs). Prevent T cell activation.
  • Rituximab – anti-CD20. Deplete mature B cells.
  • Natalizumab – anti-a4 integrin. Prevent T cell migration.
  • Tocilizumab – anti-IL-6 receptor. Reduce macrophage, T/B cell and neutrophil activation.
50
Q

What is CD20 a marker of?

A

Mature B cells

51
Q

Which biological agent targets CD20?

A

Rituximab

52
Q

What is the function of IL-2?

A

Activates T cells

53
Q

What is the mechanism of action of natalizumab?

A

Antibody against a2 integrin

Prevents leukocyte migration

54
Q

What class of drugs are infliximab, adalimumab, certolizumab, golimumab?

A

Anti TNFa antibodies

55
Q 
What is:
Etanercept?
Ustekinumab?
Secukinumab?
Denosumab?
A
  • TNFa antagonist, made of TNF receptor p65-Ig fusion protein
  • Antibody against p40 subunit of IL12 and IL23
  • Antibody against IL17
  • Antibody against RANK-Ligand
56
Q

Which cells express RANK?

A

Osteoclasts

57
Q

What is the risk of denosumab?

A

Avascular necrosis (of the jaw)

58
Q

What cell type does JC virus infect, and what does infection put a patient at risk of?

A

Oligodendrocytes

Progressive multifocal leukoencephalopathy

59
Q

What is the pathophysiology of anaphylaxis?

A

Cross-linking of IgE on surface of mast cells –> degranulation –> histamine, leukotrienes

• Increase vascular permeability, smooth muscle contraction, inflammation, mucus production

60
Q

What is the immediate management of anaphylaxis?

A

• Respiratory support may be required – intubation, tracheostomy
• Oxygen by mask
• Adrenaline IM 0.5mg, maybe repeat
o Increase BP, limit vascular leakage, bronchodilate
• Chlorpheniramine (antihistamine) IV 10mg
• Nebulized bronchodilators
• Hydrocortisone 200mg IV
o Systemic anti-inflammatory agent
o ~30 mins to take effect and doesn’t peak for several hours
o Important in preventing rebound anaphylaxis
• IV fluids

61
Q

When is desensitisation (aka immunotherapy) useful?

A

insect venom and some aero-allergens (e.g. grass pollen)

62
Q

What does complement deficiency put one at risk of?

A

Infection by encapsulated organisms: pneumococcus, meningococcus, gonococcus, haemophilus influenza B

63
Q

What does antibody deficiency put one at risk of?

A

recurrent bacterial infections, esp upper and lower respiratory tract

64
Q

Which immunological investigation to assess complement function?

A

C3 and C4, CH50, AP50

65
Q

What does the CH50 test?

A

All components of the classical pathway of complement activation.
C1,4,2
C3
C5-9

66
Q

What does the AP50 test?

A

All components of the alternative pathway of complement activation.
properdin, factor B/H/I
C3
C5-9

67
Q

How would you manage someone with a complement deficiency?

A
  • Meningovax, pneumovax, HIB vaccines

* Daily prophylactic penicillin

68
Q

Which serological markers reflect disease activity in SLE?

A

dsDNA antibody titre
ESR
Low levels of C4 and C3 (suggests active SLE)

69
Q

Why is C4 and C3 low in active SLE?

A
  • Immune complexes bind to C1q and activate classical pathway of complement activation
  • Complement is consumed
70
Q

What pattern of nephritis is seen in SLE?

A

Diffuse proliferative nephritis

71
Q

What does a low C3 and C4 generally indicate?

A

Activation of the classical complement pathway

72
Q

How do lymphoproliferative disorders cause anaemia?

A
  • Space limitation: expansion of malignant clone crowds out normal red and white cell precursors
  • Inhibitors: tumoru may produce local cytokines to inhibit normal bone marrow function
73
Q

Which genetic factors predispose to RA?

A 
HLA DR4 and HLA DR1
PADI (peptidylarginine deiminase) type 2 and type 4
PTPN 22 (Protein tyrosine phosphatase non-receptor 22)
74
Q

What is the 1st line treatment for RA?

A

Methotrexate

Pathology (5 decks)

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